Semaglutide and tirzepatide lower pulmonary artery pressure in heart failure patients with implanted sensors
A Yale led retrospective study of 60 heart failure patients with implanted pressure sensors found lower pulmonary artery pressure six months after starting semaglutide or tirzepatide, and fewer heart failure hospitalisations in the following year.
What's new
A Yale led analysis of 60 heart failure patients with CardioMEMS sensors found pulmonary artery pressure fell after starting semaglutide or tirzepatide, and yearly heart failure admissions dropped from 1.2 to 0.3 per patient.
Why it matters
It gives a direct pressure measurement to support outcome trials such as SUMMIT, but the design has no control group and may overstate the fall in admissions.
What's next
The authors called for research on mechanisms; full publication and a randomised sensor study would test whether the drugs cause the change.
Starting semaglutide or tirzepatide was followed by a drop in pulmonary artery pressure in people with heart failure and obesity who carried an implanted pressure sensor, a retrospective study presented at the Heart Failure Society of America meeting reports. Heart failure hospitalisations fell from 1.2 to 0.3 per patient per year when the year after treatment began was compared with the year before. The study had 60 patients and no control group. It adds a measured pressure signal to a field where most evidence so far comes from symptoms and outcome trials.
What the sensor study measured
The analysis was presented at the society's annual scientific meeting in Phoenix, held October 9 to 12, 2026, and described by Christopher Maulion of the Yale School of Medicine, according to a report in HCPLive. The team searched a Yale health system database for heart failure patients who had a CardioMEMS sensor, a small wireless device placed in a branch of the pulmonary artery that lets clinics track pressure remotely. Of 506 patients with the implant, 60 had taken semaglutide or tirzepatide for at least six months and were included. Forty eight took semaglutide and twelve took tirzepatide. Pressures, weight, diuretic use and blood markers were compared at the start, at three months and at six months.
The patients were on average 63.7 years old, and 65% were men. Average body weight at the start was 116 kilograms, and average pulmonary artery systolic pressure was 46 mmHg. Cardiac events, including heart failure hospitalisations and urgent care visits, were counted for one year before and one year after each patient started the drug. This design means every patient served as their own comparison. It avoids some differences between groups, but it cannot rule out other changes in care over the same period. The report did not say how many patients had heart failure with preserved or with reduced ejection fraction, a split that matters for how the results apply.
Pressure and hospitalisation results
At six months, systolic pressure in the pulmonary artery was 3.74 mmHg lower on average than at the start, after a fall of 2.75 mmHg at three months, HCPLive reported. Mean pressure fell by 2.67 mmHg and diastolic pressure by 1.7 mmHg at six months. All of these changes were statistically significant. Weight fell by 4.4% on average at six months. The share of patients on a loop diuretic dropped from 85% to 67%, although the average diuretic dose did not change significantly. The authors concluded that starting either drug substantially reduced pulmonary artery pressure in this group. The absolute changes are modest next to the spread between patients, which was wide.
Heart failure hospitalisations dropped from an average of 1.2 per patient in the year before treatment to 0.3 per patient in the year after.
The hospitalisation figure drew the most attention. Heart failure hospitalisations dropped from an average of 1.2 per patient in the year before treatment to 0.3 per patient in the year after. That is a fall of about three quarters. The link between weight loss and pressure change was weak and not statistically significant, which hints that the drugs may act on the heart and vessels through more than weight alone. The authors wrote that "limited data exist on their direct hemodynamic effects in patients with obesity and HF," and called for more research. The table sets out the main numbers as reported.
| Measure | Start | Change or result |
|---|---|---|
| Patients included | 60 of 506 with a sensor | 48 semaglutide, 12 tirzepatide |
| Systolic PA pressure | 46 mmHg | minus 3.74 mmHg at six months |
| Mean PA pressure | not reported | minus 2.67 mmHg at six months |
| Body weight | 116 kilograms | minus 4.4% at six months |
| Loop diuretic use | 85% of patients | 67% at six months |
| Heart failure hospitalisations | 1.2 per patient per year | 0.3 per patient per year |
Why a before and after design needs caution
A before and after comparison in a small, selected group is a starting point, not proof. Sensors are often implanted after recent hospital stays, so their worst year may fall just before the device and the new drug arrive. Hospitalisations can then fall partly because a bad stretch ends on its own, a pattern known as regression to the mean. Better remote monitoring from the sensor itself may also cut admissions. Only patients who stayed on the drug for at least six months were included, which leaves out anyone who stopped early because of side effects or a poor response. Readers can apply the same checks this site suggests for any weight loss trial headline.
The authors also noted that weight loss in their cohort was smaller than in earlier cardiovascular outcome trials. That may reflect real world use, lower average doses, or the shorter six month window. The tirzepatide group was small, with twelve patients, so the study cannot compare the two drugs. A head to head trial of tirzepatide and semaglutide on weight already exists, but no similar comparison has been made for heart pressures. The abstract has been presented at a meeting and has not yet appeared as a full peer reviewed paper, so details such as the statistical methods and the exact patient mix are still limited.
Where the evidence on heart failure stands
The randomised evidence is stronger for tirzepatide. In the SUMMIT trial, 731 adults with heart failure with preserved ejection fraction and a body mass index above 30 were assigned to tirzepatide or placebo for about two years. Cardiovascular death or worsening heart failure occurred in 36 patients on tirzepatide and 56 on placebo, a hazard ratio of 0.62, according to the American College of Cardiology summary. The benefit came from fewer worsening heart failure events, with no significant difference in cardiovascular death. SUMMIT measured events, not pressures inside the heart and lungs. The new sensor data add a direct measurement of pulmonary artery pressure to this outcome evidence.
The study does not change who should get these drugs. Their approved uses depend on each country's label, and heart failure patients already take several drugs whose doses may need adjusting as weight and fluid status change. The drop in diuretic use in this group points to that practical issue. Any decision to start or stop a GLP 1 or dual agonist in heart failure belongs with the treating cardiology team. The next step the authors called for is research on mechanisms, and ideally a prospective study in which sensor patients are randomised, so that falling pressures can be tied to the drug rather than to the course of the disease.
Conclusion
In 60 heart failure patients with implanted sensors, semaglutide or tirzepatide was followed by lower pulmonary artery pressure and far fewer hospital admissions over a year. The study is small, retrospective and uncontrolled, and its hospitalisation drop may partly reflect patients enrolling after a bad year. It still offers a rare direct look at heart and lung pressures on these peptides. A randomised sensor study and full publication of the data would show how much of the benefit belongs to the drugs.
